Mechanisms of inhibition of vasopressin release during moderate antiorthostatic posture change in humans

The hypothesis was tested that the carotid baroreceptor stimulation caused by a posture change from upright seated with legs horizontal (Seat) to supi ne (Sup) participates in the suppression of arginine vasopressin (AVP) rele ase. Ten healthy males underwent this posture change for 30 min without or with simultaneous application of lower body negative pressure (LBNP) adjust ed to maintain left atrial diameter (LAD) at the Seat level. Throughout Sup , mean arterial pressure and heart rate decreased from 98 +/- 2 to 91 +/- 2 mmHg and from 63 +/- 2 to 55 +/- 2 beats/min (P < 0.05), respectively, whe reas the corresponding decreases during Sup + LBNP were attenuated and of s horter duration (98 +/- 2 to 93 +/- 2 mmHg and 62 +/- 2 to 58 +/- 3 beats/m in, P < 0.05). During Sup, LAD increased from 30 +/- 1 to 33 +/-. 1 mm, and arterial pulse pressure (PP) increased from 40 +/- 2 to 47 +/- 2 mmHg, whe reas plasma AVP decreased from 0.9 +/- 0.2 to 0.5 +/- 0.1 pg/ml (P < 0.05), and plasma norepinephrine (NE) decreased from 176 +/- 20 to 125 +/- 16 pg/ ml (P < 0.05). During Sup + LBNP, there were no changes in LAD, PP, plasma AVP, or NE. In conclusion, vasopressin secretion is suppressed during an an tiorthostatic posture change, which increases carotid sinus pressure, PP, a nd LAD. The suppression is absent when PP and LAD are prevented from increa sing and is thus critically dependent on at least one of these stimuli.